The main thrust of the laboratory is focussed on the influence of pressure on the blood coagulation system, including both hemostasis and thrombosis. However, our findings emphasize the important role of the water molecule in these biochemical reactions. Platelet aggregation takes place because oppositely charged amino acids are juxtaposed at the binding site (Arg-GlyAsp-Ser). Normally, charged residues are surrounded by water (small dipolar molecules). These organized water molecules are arranged compactly around the charged residues. When this shield of water is made thinner by increased escaping tendency the oppositely charged residues interact and the volume of the solution is increased by water molecules which are randomized into the bulk phase. Platelet aggregation is inhibited by increasing the concentration of neutral salts, because counterions surround the charged residues, thus weakening the charge effect. For the same reason fibrin polymers dissolve in salt solution (1 M NaBr). Molecules having a large electric dipole moment inhibit decompression- inducible platelet aggregation (DIPA) by essentially the same mechanism as if the ionic strength were increased. This was confirmed experimentally. Piracetam (N- acetamide of GABA) has a large electric dipole moment (6.7 Debye units) which can block both fibrin polymerization and DIPA at a low concentration (1 mM); the rate of fibrin polymerization is decreased 50% by 9 mM piracetam.